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47 Cards in this Set
- Front
- Back
what is a neoplasm/neoplasia?
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- "new growth"
- abnormal mass of tissue where cells are proliferating beyond the stimuli that caused it; - often called "tumor" or bump - can be b9 or malignant |
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describe b9 neoplasm
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1- grows w/in pseudocapsule w/well demarcated borders that exerts pressure on surrounding tissue causing it to atrophy
2- has no capability to metastasize 3- named by taking parenchyma and adding "-oma" 4- well differentiated & may resemble structure of normal tissue 5- overcrowded but architecturally organized 6- rate of growth is slowly progressive & may regress where dystrophic calcification might occur 7- adenoma term used to describe epithelial neoplasms growing in glandular pattern 8- contain normal bipolar mitotic figures |
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what are examples of b9 neoplasms?
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- fibroma: b9 neoplasm of fibroblasts
- chondroma: b9 neoplasm of cartilage - osteoma: b9 neoplasm of bone |
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describe malignant neoplasm
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1- grows locally w/in pseudocapsule, invades by breaking thru pseudocapsule into surrounding tissue, then metastasizes
2- borders are not demarcated; very poorly differentiated so difficult to tell cell origin w/anaplasia 3- crowded w/unorganized architecture 4- rate of growth is off course; maybe slow to rapid but typically faster growing than b9 neoplasms 5- typically called "cancers" 6- if derived fm mesenchymal tissue called "sarcoma" 7- if derived fm 3 germ layers: ecto, endo, mesoderm tissue called "carcinoma" 8- exceptions to naming convention: mesothelioma, lymphoma, melanoma, hamartoma 9- contain multipolar mitotic figures |
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examples of malignant neoplasms?
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- fibrosarcoma
- chondrosarcoma - osteogenic sarcoma - adenocarcinoma - squamous cell carcinoma |
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what is a hamartoma?
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- mass of non-neoplastic disorganized tissue
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describe hyperplasia
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- cells are under hormonal control and proliferate in response to increased hormonal levels
- can be pathologic or physiologic |
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examples of pathologic hyperplasia?
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- BPH hormone in excess causes prostate enlargement due to cellular proliferation
- hyperplastic endometrium |
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describe metaplasia
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- when one cell type is replaced for another
- N/C ratio is low meaning cells towards the surface are mature like they shd be - crowded but architecturally organized - metaplasia named by taking name of cell it turned into and adding "metaplasia" |
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ex of metaplasia?
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- squamous metaplasia where original pseudostratified cilitated columnar cells were turned into squamous cells
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describe dysplasia
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- disorderly proliferation bc of fast replication rate w/increased no. of mutations
- unorganized architecture - high N/C ratio - antedates cancer - pleomorphic - mitotic figures present |
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ex of dysplasia?
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- carcinoma in situ: where dysplasia takes entire thickness of epithelium
- considered most severe form of dysplasia just before CA |
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what is overall progression to CA?
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metaplasia => dysplastic => b9 => malignant tumor
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what are 2 components of tumors?
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- stroma: supports parenchyma and contains lots of BVs
- parenchyma: contain the neoplastic cells of monoclonal origin which eventually become pleomorphic due to crowding and increased rate of mutation |
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what are the 3 routes of metastasis or dissemination?
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1- seeding w/in bodily cavities: favored by carcinomas
2- lymphatic spread favored by carcinomas 3- hematogenous spread favored by sarcomas |
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what is angiolymphatic invasion?
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- when malignant neoplasm spreads to lymphatics and blood vessels
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ex of seeding w/in body cavities
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- ovarian cancer: which can spread to abdominal cavity
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ex of lymphatic spread
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- breast cancer spreads to axillary lymph nodes
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describe retinoblastoma
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- CA by heredity;
- autosomal dominant |
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describe adeonomatous polyposis coli
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- CA by heredity
- autosomal dominant - several small polyps form |
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describe xeroderma pigmentosum
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- CA by heredity
- autosomal recessive - sun-induced skin CA - defect in DNA repair enzyme |
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what are some CA influenced by the environment?
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- stomach CA
- hepatocellular CA - Cervical CA; HPV associated |
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but what are most CAs?
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- non-familial & occur sporadically
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what are oncogenes?what do they produce?
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- are proto-oncogenes that have mutated
- they promote autonomous cell growth in CA - they produce oncoproteins that resemble normal products of oncogenes |
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what is carcinogenesis?
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- is non-lethal genetic damage/mutation
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what causes carcinogenesis?
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- virus
- radiation - chemical - inherited - cumulative replication errors |
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how does CA originate?
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- fm single progenitor(origin) that undergoes monoclonal expansion later on turning into pleomorphic cells due to crowding and mutation
- CA can evolve phenotypically & genotypically |
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what are the genes damaged in order to CA?
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- growth promoting proto-oncogenes
- cancer suppressor genes - apoptosis regulating genes - genes encoding DNA repair proteins |
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what are proto-oncogenes?
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- are genes that dont directly affect cell proliferation but an indirect effect so that when mutated they have effect on cell proliferation
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what are non-oncogenic genes?
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- are genes that have nothing to do w/cellular proliferation
Ex: keratin |
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what are the oncoproteins produced by oncogenes?
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-oncoproteins resemble the normal products produced by proto-oncogenes but difference there's no regulation
- growth factors - growth factor receptors - signal transducing proteins critical for mitosis |
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describe growth factors as oncoproteins
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- where growth factors continuously bind one after another causing over expression of the gene
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describe growth factor receptors as oncoproteins
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- where receptor gets stuck "on" and generates continuous mitotic signal
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ex of growth factor receptors as oncoproteins
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- EGF gene, c-erb B-1
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what are signal transducing proteins?
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- are intermediates btw receptor and nucleus
- responsible for transducing the signal that will be sent to nucleus for it to divide/undergo mitosis |
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describe c-ras gene
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- aka"GTP/G binding protein"
- located on inside of membrane - encodes GTP binding protein which signal mitosis - contains a GTPase that becomes active w/help of GAP protein to shut off |
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what happens when there is a point mutation in ras gene?
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- makes GTPase useless causing unregulated mitosis and cause nasty CAs ie colon CA, pancreas, lung CA)
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what are the ways oncogenes become activated?
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1- point mutations : ie ras protein
2- chromosomal translocations: Ex specifically reciprocal translocation of chromosomes 9 & 22 which causes makes a hybrid gene that makes tyrosine kinase which leads to chronic myelogenous leukemia 3- gene amplification Ex: N-myc protein causes neuroblastoma |
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what are some cancer suppressor genes?
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- growth inhibitory factors
- molecules that regulate cell adhesion - molecules that regulate signal transduction - molecules that regulate nuclear transcription & cell cycle |
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ex of molec that regulates cell adhesion
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- E-cadherin
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ex of molec that regulates signal transduction
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- NF-1 gene
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ex of molec that regulates cell cycle & transcription
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- rbg protein
unphosphorylated state = hypophosphorylated active state |
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how does HPV take advantage?
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- when mutation occurs to rbg protein it no longer binds to transcription proteins, so HPV grabs these floating and makes its virus
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what genes regulate apoptosis?
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- bcl-2 and bax favors genes
- bcl-2 favors immortality - bax favors apoptosis |
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what results fm over expression of bcl-2, and bax?
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- bcl-2 causes large B-cell lymphoma
- overexpression bax=cell death |
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what is meant by mulitstep carcinogenesis?
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- meaning no single oncogene can directly cause CA its just the accumulation of mutations
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what are elements involved in kinetics of tumor cell growth?
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- tumor cell doubling time
- growth fraction: are portion of cells in the mitotic cycle - cell production vs cell loss |